Mechanism of increased inspiratory rib elevation in ascites.

The detrimental effect of ascites on the lung-expanding action of the diaphragm is partly compensated for by an increase in the inspiratory elevation of the ribs, but the mechanism of this increase is uncertain. To identify this mechanism, the effect of ascites on the response of rib 4 to isolated phrenic nerve stimulation was first assessed in four dogs with bilateral pneumothoraces. Stimulation did not produce any axial displacement of the rib (X(r)) in the control condition and caused a cranial rib displacement in the presence of ascites. This displacement, however, was small. In a second experiment, the effects of ascites on the pleural pressure swing (DeltaP(pl)), intercostal activity, and X(r) during spontaneous inspiration were measured in eight animals. As the volume of ascites increased from 0 to 200 ml/kg body wt, X(r) increased from 3.5 +/- 0.5 to 7.5 +/- 0.9 mm (P < 0.001), DeltaP(pl) decreased from -6.4 +/- 0.4 to -3.6 +/- 0.3 cmH(2)0 (P < 0.001), and parasternal intercostal activity increased 61 +/- 19% (P < 0.001). The role of the decrease in DeltaP(pl) in causing the increase in X(r) was then separated from that of the increase in intercostal muscle force using the relation between X(r) and DeltaP(pl) during passive lung inflation. The loss in DeltaP(pl) accounted for two-thirds of the increase in X(r). These observations indicate that 1) the increased inspiratory elevation of the ribs in ascites is not the result of the increase in the rib cage-expanding action of the diaphragm and 2) it is due mostly to the decrease in DeltaP(pl) and partly to the increase in the force exerted by the parasternal intercostals on the ribs. These observations also suggest, however, that the rib cage expansion caused by ascites makes the parasternal intercostals less effective in pulling the ribs cranially.